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38 publications mentioning rno-mir-19a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-19a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 216
Figure 5(A) Real-time quantitative PCR demonstrated that transfection of cardiomyocytes with miR-19a-3p mimics increased the expression of miR-19a-3p level, while miR-19a-3p inhibitor reduced the expression of miR-19a-3p level, but SFI increased the expression of miR-19a-3p level (**P < 0.01, n = 3 for each group). [score:9]
Cells were divided into six groups: control group (normal cardiomyocytes), PE + NC group (PE mo del transfected with negative control), PE + miR19 mimics group (PE mo del transfected with miR-19a-3p mimics), PE + miR19 inhibitor group (PE mo del transfected with miR-19a-3p inhibitor), PE + miR19 mimics + SFI group (PE mo del transfected with miR-19a-3p mimics, and treated with SFI 10 um/ml) and PE + miR19 inhibitor + SFI group (PE mo del transfected with miR-19a-3p inhibitor, and treated with SFI 10 um/ml). [score:9]
The result of qRT-PCR analysis showed that the expression level of miR-19a-3p increased by 3.68-fold and 3.48-fold when the cardiomyocytes were treated with 10 um/ml SFI and transfected with miR-19a-3p mimic or miR-19a-3p inhibitor for 48 h respectively, as compared with NC group (p < 0.01) (Fig.   5A); the level of MEF2A mRNA was down-regulated by 49% and 40% respectively (p < 0.01) (Fig.   5B); the cell size both reduced by 20% (p < 0.01) (Fig.   5C) As demonstrated in Fig.   6, in both AAC -induced hypertrophic myocardium and PE -induced hypertrophic myocyte mo del, the protein expressions of MEF2A, β-MHC, BNP and TRPC1 were all increased significantly as compared with those in sham-operation or control group (p < 0.01), while there was no significant difference between SFI and control groups (Fig.   6A,B). [score:8]
The specific mimic or inhibitor RNA was transfected to overexpress or knock down miR-19a-3p expression. [score:8]
Our data suggest that MEF2A is a target of miR-19a-3p, and miR-19a-3p up-regulation could reduce the expression of MEF2A mRNA and protein. [score:8]
Overall, these results revealed that miR-19a-3p could directly target and regulate the expression of MEF2A. [score:7]
Furthermore, lower -expression of miR-19a-3p may enhance the expression of MEF2A, β-MHC, BNP and TRPC1 in cardiomyocyte hypertrophy, which seemingly implies that lower -expression of miR-19a-3p mediated MEF2 signaling might be a cause of myocardial hypertrophy. [score:7]
We suppose that SFI attenuates myocardial hypertrophy by upregulating the levels of particular miRNAs, including miR-19a-3p, miR-181d-5p, miR-210-3p, miR-352 and miR-324-3p, and downregulating miR-199a-5p. [score:7]
For the first time, we discovered that SFI could attenuate myocardial hypertrophy, probably through up -regulating or maintaining the miR-19a-3p level, decreasing MEF2A mRNA and protein expressions, and regulating the protein expression of β-MHC, BNP and TRPC1 of the MEF2 signaling pathway. [score:7]
Interestingly, our study showed that MEF2A was the target gene of miR-19a-3p, and it was highly expressed in the hypertrophic myocardium mo del under lower -expression of miR-19a-3p. [score:7]
To examine whether miR-19a-3p regulated the expression of MEF2A, a predicted target of miR-19a-3p, the dual luciferase psiCheck2 reporter plasmid (Promega, Madison, WI, USA), was used to generate the reporter plasmid harboring MEF2A 3′-UTR. [score:6]
Our study suggested that SFI attenuated myocardial hypertrophy probably by enhancing the expression of miR-19a-3p and down -regulating the expression of MEF2A, β-MHC, BNP and TRPC1, which seemingly implies that the SFI mediated improvement within MEF2 signaling might be the cause of attenuated myocardial hypertrophy. [score:6]
miR-19a-3p inhibitor was sufficient to knock down endogenous miR-19a-3p expression in cultured cardiomyocytes as analyzed by qRT-PCR (p < 0.01) (Fig.   5A). [score:6]
In addition, viral -mediated overexpression of miR-19a-3p in the rat hypertrophy mo del would help understand how relevant SFI -induced upregulation of this miRNA attenuates hypertrophy, and help optimize our in vivo experimental studies in further. [score:6]
In our current study, the regulation of miR-19a-3p expression only represents one action of SFI’s targets. [score:6]
Compared with the negative control RNA, the miR-19a-3p mimic significantly suppressed the activity of the luciferase reporter fused with MEF2A 3′-UTR by 37% (Fig.   3D), suggesting that miR-19a-3p inhibited MEF2A expression through its 3′-UTR. [score:6]
The Western blot result showed that MEF2A was down-regulated, while anti-miR-19a-3p promoted MEF2A expression (Fig.   3E,F). [score:6]
SFI reduces cell size, increases the expression level of miR-19a-3p and MEF2A mRNA after transfection with miR-19a-3p mimic or inhibitor. [score:5]
The results showed that the level of MEF2A mRNA was markedly down-regulated by 36% in miR-19a-3p overexpression cardiomyocytes compared with NC (p < 0.01) (Fig.   5B). [score:5]
To explore the mechanism by which miR-19a-3p affected cardiomyocyte hypertrophy, we searched potential targets of miR-19a-3p using bioinformatic algorithms, such as MiRanda, Pictar and TargetScan. [score:5]
The levels of the above-mentioned proteins were decreased significantly in the clones infected with miR-19a-3p mimic in PE -induced hypertrophic myocytes (p < 0.01), among which the protein expression of MEF2A, β-MHC, BNP and TRPC1 all increased significantly in the clones infected with miR-19a-3p inhibitor (p < 0.01). [score:5]
We further examined the expression of MEF2A, one confirmed target of miR-19a-3p, along with mRNA levels by qRT-PCR. [score:5]
Compared with the miR-19a-3p mimic, the level of MEF2A mRNA was markedly up-regulated by 40% in miR-19a-3p lower -expression cardiomyocytes compared with miR-19a-3p mimic (p < 0.01) (Fig.   5B). [score:4]
miR-19a-3p was significantly down-regulated in AAC 12-week hearts. [score:4]
Interestingly, the increase in miR-19a-3p expression was most pronounced in SFI group, by 0.58 fold (Fig.   3B). [score:3]
Over -expression of miR-19a-3p in the myocardium may prove to be able to attenuate myocardial hypertrophy. [score:3]
It was found in our study that the most striking change was the miR-19a-3p expression in mo del group. [score:3]
Figure 3MEF2A is the target gene of miR-19a-3p. [score:3]
MEF2A is a target gene of miR-19a-3p. [score:3]
We found that miR-19a-3p expression underwent a change after myocardial hypertrophy. [score:3]
293 T cells were co -transfected with the psiCheck2 vector containing MEF2A 3′-UTR and miR-19a-3p mimic using Lipofectamine 2000 (Invitrogen, Carlsbad, CA,USA), and the co-transfection with non -targeting negative control RNA was performed as control. [score:3]
The size of cardiomyocytes transfected with miR-19a-3p inhibitor increased by 26% in culture medium with PE (100 mM) (p < 0.01) (Fig.   5C). [score:3]
Lower -expression of miR-19a-3p increased the cell size (100 mM). [score:3]
SFI reduced the cell size either transfected with miR-19a-3p mimics or inhibitor. [score:3]
qRT-PCR analysis demonstrated that transfection of cardiomyocytes with miR-19a-3p mimics increased the expression of miR-19a-3p level (p < 0.01) (Fig.   5A). [score:3]
Analysis of the functional impact of individual change on miR-19a-3p expression in the myocardium revealed that it had a beneficial effect on the maintenance of a normal physiological state. [score:3]
MEF2A is inhibited by miR-19a-3p under physiological conditions, and during the myocardial hypertrophy process as well. [score:3]
Myocytes specific enhancer factor 2A (MEF2A), a critical executioner of cardiac hypertrophy, was predicted as a putative target of miR-19a-3p. [score:3]
To investigate whether endogenous miR-19a-3p played a significant role in cardiomyocytes, antisense oligonucleotidemediated miRNA knockdown was performed using miR-19a-3p inhibitor to knock down the endogenous miR-19a-3p. [score:3]
PE+ miR-19a-3p inhibitor. [score:3]
The normalized curve method was used to determine the linked expression level of the mRNAs and miR-19a-3p, which was standardized to GAPDH and U6, respectively. [score:3]
These results also imply that miR-19a-3p may regulate MEF2-related genes. [score:2]
When cardiomyocytes were transfected with miR-19a-3p mimic or NC for 48 h, up-regulation of miR-19a-3p reduced the cell size by 17% as measured by cardiomyocyte immunochemistry and cell surface area (p < 0.01) (Fig.   5C). [score:2]
We suppose that dysregulation and function of miR-19a-3p in the myocardium play an important role in myocardial hypertrophy. [score:2]
Our primary research question was how myocardial miR-19a-3p played a role in the MEF2 signaling pathway. [score:1]
Atrial natriuretic peptide (ANP), β-myosin heavy chain gene (MYH7) and myocytes specific enhancer factor 2A (MEF2A) mRNA levels and miR-19a-3p levels in the myocardial tissues and/or cardiomyocytes were determined by qRT-PCR. [score:1]
miR-19a-3p mimics. [score:1]
As shown in Fig.   3B and C, miR-19a-3p levels were decreased by 0.69 fold in mo del group after abdominal aortic constriction (AAC). [score:1]
The identification of one miR-19a-3p -binding site was done in the 3′ -UTR of MEF2A mRNA (Fig.   3A). [score:1]
miR-19a-3p and MEF2A mRNA levels were determined. [score:1]
PE+ miR-19a-3p mimics. [score:1]
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[+] score: 191
In addition, H/R stimulation increased the expression of Bax and down-regulated the expression of Bcl-2. Overexpression of miR-19a markedly reversed the effect on the expression levels of Bcl-2 and Bax in the cells exposed to H/R. [score:12]
We verified that overexpression of miR-19a inhibited PTEN expression and initiated the PI3K/Akt pathway, resulting in down-regulation of apoptosis. [score:10]
Because miR-19a expression was inhibited by H/R in H9C2 cells and we observed that cell viability was decreased in the H/R group, whereas overexpression of miR-19a inhibited the reduction in the cell induced by H/R injury, we wondered whether miR-19a protected cardiomyocyte against H/R -induced cell apoptosis. [score:9]
miR-19a reduces H/R -induced cell apoptosisBecause miR-19a expression was inhibited by H/R in H9C2 cells and we observed that cell viability was decreased in the H/R group, whereas overexpression of miR-19a inhibited the reduction in the cell induced by H/R injury, we wondered whether miR-19a protected cardiomyocyte against H/R -induced cell apoptosis. [score:9]
As the Figure shows, the expression of PTEN was decreased and p-Akt increased after miR-19a up-regulation (Figure 5C). [score:6]
In the present study, we confirmed that miR-19a expression was dramatically down-regulated in H9C2 cells during hypoxia/reoxygenation (H/R) injury. [score:6]
All these findings suggested that miR-19a inhibited PTEN expression by directly binding to its 3′-UTR. [score:6]
Figure 1The expression of miR-19a in H9C2 cells by qRT-PCR after H/R treatmentData are expressed as mean ± S. D. (n=3). [score:5]
After transfection of miR-19a mimic, the expression of PTEN decreased, while the p-Akt expression was increased (Figure 5A,B). [score:5]
PTEN is a potential target of miR-19a In order to elucidate the underlying molecular mechanism, we performed a bioinformatic analysis using ‘TargetScan’. [score:5]
miRNA target prediction program revealed PTEN as one of the possible target genes of miR-19a. [score:5]
Expression of miR-19a was overtly reduced by reaching a inhibition of 40.48% in H9C2 after H/R treatment compared with normoxia group (P<0.05) (Figure 1). [score:4]
We examined the role of miR-19a up-regulation in H/R -induced cardiomyocyte injury. [score:4]
For luciferase assays, the potential miR-19a -binding site in the PTEN 3′-UTR was predicted by miRNA target prediction databases, including Miranda, TargetScan, and PicTar. [score:4]
So, our results showed that miR-19a can regulate via a PTEN/Akt pathway in H9C2 cells, which inhibits cardiomyocyte apoptosis during H/R injury. [score:4]
Effect of miR-19a on cell survival in H/R -induced cardiomyocyte injuryWe examined the role of miR-19a up-regulation in H/R -induced cardiomyocyte injury. [score:4]
The expression of miR-19a in H9C2 cells by qRT-PCR after H/R treatment. [score:3]
After 24-h exposure to hypoxia and 3-h reoxygenation, the LDH release was increased in the culture medium (Figure 2B), the relative amount of LDH release reached 133.6% of that in control group (* P<0.05) (Figure 2B), and the miR-19a up-regulation group significantly decreased LDH release ([#] P<0.05 compared with H/R + NC group). [score:3]
In summary, the present study provided evidence that miR-19a can decrease cardiomyocyte apoptosis induced by H/R via inhibiting PTEN and increasing nuclear AKT. [score:3]
Our study demonstrated that H/R -induced injury of H9C2 cells was significantly inhibited by miR-19a pretreatment. [score:3]
PTEN is a potential target of miR-19a. [score:3]
miR-19a may be a potential drug target for treating cardiomyocyte I/R injury. [score:3]
miR-19a expression in H9C2 after H/RTo identify the potential effect of miR-19a in myocardial I/R injury, we measured the expression of miR-19a in H9C2 cells after 24-h hypoxia and 3-h reoxygenation. [score:3]
from the experiments showed that H/R treatment significantly decreased cell viability and increased LDH release in the culture medium, whereas overexpression of miR-19a efficiently promoted cell growth and decreased LDH release. [score:3]
So, our results showed that H/R injury resulted in increase in apoptosis and overexpression of miR-19a may be responsible for decreasing apoptosis and protecting cardiomyocyte during H/R injury, which is consistent with the results of other studies [37, 38]. [score:3]
Effect of miR-19a on PTEN/p-Akt pathway in H/R cardiomyocytesPTEN is traditionally known to generate effects via suppression of p-Akt. [score:3]
Furthermore, transfection of miR-19a resulted in significant reduction in PTEN mRNA and protein expression by real-time RT-PCR and Western blotting analysis (Figure 4D,E). [score:3]
Therefore, we can assume that PTEN is a functional target gene of miR-19a involved in protecting cardiomyocyte injury in myocardial I/R. [score:3]
miR-19a is previously confirmed to be an important regulator in heart development. [score:3]
Figure 4 miR-19a targets PTEN(A) The potential binding site for miR-19a in the 3′-UTR of PTEN mRNA. [score:3]
Here, we explored the expression changes of miR-19a during myocardial H/R injury. [score:3]
miR-19a expression in H9C2 after H/R. [score:3]
miR-19a targets PTEN. [score:3]
According to bioinformatic analyses, PTEN was regarded as a target of miR-19a. [score:3]
PTEN may be the target gene of miR-19a against H/R -mediated cardiomyocyte apoptosis. [score:3]
Regulation of the PTEN/p-Akt pathway by miR-19a. [score:2]
We sought to examine the significance of miR-19a -mediated regulation of the PTEN//PI3K/p-Akt signaling pathway in H9C2 cells during H/R injury. [score:2]
Figure 5Regulation of the PTEN/p-Akt pathway by miR-19a(A) Real-time PCR analysis of PTEN in H9C2 cells. [score:2]
In our studies, it was found that H/R injury resulted in reduction by 47.5% of the expression of miR-19a after 24-h hypoxia and 3-h reoxygenation as compared with controls. [score:2]
However, little information is available regarding the effects of miR-19a on hypoxic adaptation in cardiomyocytes. [score:1]
The impact of miR-19a on PTEN expression was normalized and compared with the negative miRNA (n=3), * P<0.05 compared with the wt + negative miRNA group. [score:1]
Effects of miR-19a on H/R -induced apoptosis in H9C2 cells. [score:1]
Effect of miR-19a on cell survival in H/R -induced cardiomyocyte injury. [score:1]
miR-19a reduces H/R -induced cell apoptosis. [score:1]
Moreover, flow cytometry revealed that the H/R -treated cells showed greater apoptosis than control, whereas miR-19a pretreatment reversed these effects. [score:1]
Then, the cells were transfected with the miR-19a mimic (50 nM) or a negative control RNA (50 nM) using Lipofectamine 2000 (Invitrogen) according to the manufacturer’s protocols. [score:1]
Together, these data indicated that miR-19a ameliorates H/R -induced cardiomyocyte injury. [score:1]
Figure 3Effects of miR-19a on H/R -induced apoptosis in H9C2 cells(A) Cells were stained with antibody to Annexin V–FITC and propidium iodide after transfection with miR-19a mimic; representative flow cytometry of apoptosis of cardiomyocyte under different conditions. [score:1]
Effect of miR-19a on PTEN/p-Akt pathway in H/R cardiomyocytes. [score:1]
dsDNA oligonucleotides containing the miR-19a -binding sequence (wild-type) or a mismatch sequence (mutant) of the 3′-UTR of PTEN mRNAs and the HindIII and SpeI restriction site overhangs were amplified using PCR method. [score:1]
The precursor of miR-19a, the negative control miRNA, and the transfection kit (Lipofectamine 2000) were purchased from Invitrogen (Carlsbad, CA). [score:1]
pMIR-REPORT constructs (100 ng) together with 1 ng of Renilla luciferase plasmid phRL-SV40 (Promega) and 50 nM of miR-19a were transfected by Lipofectamine 2000 (Invitrogen). [score:1]
Therefore, there is a close association of circulating miR-19a levels with susceptibility to AMI, and has a highly predictive and distinguishing ability. [score:1]
Values are means ± S. E. M. To identify the potential effect of miR-19a in myocardial I/R injury, we measured the expression of miR-19a in H9C2 cells after 24-h hypoxia and 3-h reoxygenation. [score:1]
Zhong et al. [32] revealed that the levels of plasma miR-19a in acute myocardial infarction (AMI) were 120-fold higher than control group and reached the level of a highly detectable. [score:1]
Therefore, miR-19a is an H/R -induced myocardial cell injury related miRNA in cardiomyocyte. [score:1]
Further, we explored the potential role of miR-19a in H/R -induced myocardial cell injury. [score:1]
In summary, the results implied that miR-19a can signal through the PTEN/Akt axis in the H9C2 cells during H/R injury. [score:1]
Figure 3C shows a higher ratio of Bcl-2 to Bax in the (miR-19a + H/R) group than in the (H/R + NC) group (P<0.05). [score:1]
Further research in human clinical trials is necessary to pave the way for miR-19a ultimate application in the clinic to benefit myocardial I/R patients. [score:1]
To confirm this hypothesis, we constructed a reporter vector consisting of the luciferase-coding sequence followed by the 3′-UTR of PTEN (wild-type and mutant type) and co -transfected miR-19a mimics with the vector in 293T cells. [score:1]
We found that PTEN contained theoretical miR-19a -binding site in its 3′-UTR (Figure 4A). [score:1]
Moreover, in the present study we found that the protein and mRNA levels of PTEN were increased and the p-Akt was decreased by H/R injury, whereas miR-19a pretreatment reversed these effects. [score:1]
We also constructed a vector in which miR-19a -binding sites were all mutated; miR-19a mimics failed to decrease the activity of luciferase gene with mutant 3′-UTR (Figure 4B,C). [score:1]
Chen and Li [21] found that the plasma concentrations of miR-19a were significantly higher in pulmonary arterial hypertension (PAH) patients than in controls; circulating miR-19a was found to be a potential, independent biomarker for diagnosis of PAH. [score:1]
Effects of miR-19a on H/R -induced injury in H9C2 cells. [score:1]
This finding raised the possibility that miR-19a may play an important role in H/R injury of H9C2 cells. [score:1]
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[+] score: 73
As shown in Figure 9A, the Arc -targeting microRNAs (miR-19a, -32a, -326, -193a), exhibited SN/homogenate expression ratios near 1 and were all significantly different from snoRNA with an expression ratio of 0.15. [score:7]
Co -expression of miR-34a with miR-19a, miR-378, or miR-326 did not modulate the inhibition induced by miR-34a expression alone. [score:7]
Using the wildtype Arc 3′UTR, we independently confirmed inhibition of reporter expression by the candidates selected from Figure 1A and further demonstrated inhibition by miR-19a and miR-326 (Figure 2A). [score:7]
In contrast, Arc -regulating miR-34a, miR-326, miR-19 and miR-193a were not significantly regulated, although there was trend for miR-34a upregulation at 30 minutes post-BDNF (p = 0.07). [score:6]
A significant difference in luciferase expression was observed after substitution mutation or deletion of the miRNA binding sites for miR-19a, miR-34a and miR-326 in response to expression of the respective miRNAs, relative to the wildtype Arc 3′UTR. [score:6]
Inhibition of the Arc 3′UTR by miR-326 was not affected by co-transfection with miR-19a, yet significantly stronger inhibition was obtained when miR-326 was paired with miR-193a or miR-378. [score:5]
In situ hybridization confirms miRNA expression in adult dentate granule cells and hippocampal pyramidal cells, while qPCR analysis shows enhanced expression of miR-19a, miR-34a, and miR-326 in synaptoneurosomes relative to cell body restricted, small nucleolar RNA. [score:5]
Mutations in the seed region of three miRNAs (miR-34a, miR-326, and miR-19a) partially or fully rescue reporter expression. [score:4]
For overexpression of miR-19a precursor a commercial construct (RmiR6091-MR04) was used (GeneCopoeia, Rockville, MD). [score:3]
miR-19a and miR-326 were added to this analysis because TargetScan (Release 6.0; November, 2011) shows a vertebrate-conserved binding site for miR-19a and two binding sites for miR-326 in the Arc 3′UTR. [score:3]
Thus, at DIV10, expression of miR-19a, miR-34a, miR-326 and miR-193a were decreased while Arc mRNA was elevated. [score:3]
Collating results from mutation studies in HEK cells with effects of miRNA manipulation in hippocampal neurons, we provide evidence that miR-19a, miR-34a, miR-193a, and miR-326 are capable of modulating Arc. [score:2]
Interestingly miR-19, miR-34 and miR-326 are all dysregulated in multiple sclerosis patients [62]. [score:2]
Dramatic changes in mature miR-19a, miR-34a, miR-326 and miR-193a were observed during development, with maximum changes of more than 100-fold. [score:2]
In contrast, miR-19a, miR-34a, miR-326 and miR-193a were not significantly regulated. [score:2]
For reasons unclear the substitution mutation procedure did not work for miR-19a. [score:2]
PNA modified antisense oligonucleotides (PNA-AS) complementary to miR-326, miR-34a and miR-19a were purchased from Panagene Inc. [score:1]
While little is currently known about mir-193a and miR-19a, new studies have shed light on miR-34 and miR-326 function in the nervous system. [score:1]
B) Quantitative relative real-time PCR of miR-19a, miR-34a, miR-326, miR-193a and miR-132. [score:1]
The effects of miR-19a and miR-34a and miR-326 is dependent on intact microRNA binding sites. [score:1]
Three nucleotides in the seed -binding region of miR-34, -193, -326, -378 and -512_5p were mutated in the Arc 3′UTR and the whole seed binding region was removed for miR-19. [score:1]
The microRNAs included were miR-19a, miR-34a, miR-193a and miR-326. [score:1]
However, complete deletion of the miR-19a seed resulted in a significant increase in reporter activity relative to wildtype. [score:1]
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[+] score: 67
Rno-miR-19a, rno-miR-19b-2 and rno-miR-214 were downregulated at all four time-points, while rno-miR-137 was downregulated at T1 followed by upregulation from T2 to T4 (Fig.   6). [score:10]
Furthermore, we observed downregulated expression of miR-19a and miR-214, which are predicted to target ARC. [score:8]
The expression of four miRNAs (rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214) and their target genes (EGR2 and ARC) were shown to be regulated by propofol in primary cultured embryonic NSCs. [score:6]
Rno-miR-19a (Rno, Rattus Norvegicus) and rno-miR-137, and their target gene EGR2, as well as rno-miR-19b-2 and rno-miR-214 and their target gene ARC were found to be closely related to neural developmental processes, including proliferation, differentiation, and maturation of NSCs. [score:6]
Another study conducted in a murine stroke mo del confirmed that miR-19a upregulation promotes NSC proliferation by targeting PTEN [46]. [score:6]
The results of the present study indicate that propofol may have the ability to regulate the expression of rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214 and their target genes, ARC and EGR2. [score:6]
It can be speculated that the increased expression of ARC in NSCs following exposure to propofol will have a beneficial effect, which is in conflict with the neurotoxic effects of propofol in vivo reported by Krzisch et al. [10] Furthermore, when combined the patterns of miR-19a and miR-214 expression, the situation is much more complex and the results are somewhat contradictory. [score:5]
MiR-19 of the miR-17–92 cluster promotes NSC proliferation [15] and targets FoxO1 to regulate NSC differentiation through cooperation with the Notch signaling pathway [16]. [score:4]
Fig. 6Quantitative RT-PCR analysis of relative expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214. [score:3]
Relative expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214 at all four time-points (immediately (T1), Day 1 (T2), Day 3 (T3) and Day 7 (T4) after treatment with propofol or DMSO). [score:3]
The fold-change in the mean expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214 ranged from -2.56 to -12.15, -2.02 to 4.61, -2.33 to -6.68 and -2.16 to -4.63, respectively (Table  5). [score:3]
In this way, we confirmed two genes (EGR2 and ARC) and four miRNAs (rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214) that exhibited at least a 2-fold change in the mean expression level following propofol treatment at all four time-points. [score:3]
MiR-19b is a member of miR-19 family located in the miR-106–25 cluster, which has been reported to be involved in regulating NSC proliferation and differentiation through a network related to the insulin/IGF-FoxO pathway [37]. [score:2]
MiR-19a is located in the miR-17–92 cluster, which promotes the NSC proliferation via repression of PTEN [15]. [score:1]
The miRNAs predicted by all four databases (rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214, (Rno, Rattus Norvegicus)) were selected for validation (Table  4 and Fig.   5). [score:1]
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[+] score: 46
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
Treatment of MLTC-1 cells with Bt [2]cAMP for 6 h increased the expression of miRNA-212, miRNA-183, miRNA-132, miRNA-182 and miRNA-96, and inhibited the expression of miRNA-138 and miRNA-19a. [score:7]
Treatment of MLTC-1 cells with Bt [2]cAMP for 6 h increased the expression of miRNA-212, miRNA-183, miRNA-132, miRNA-182 and miRNA-96 and inhibited the expression of miRNA-138 and miRNA-19a (Fig. 4B ). [score:7]
Bt [2]cAMP stimulation of granulosa cells caused down-regulation of a majority of miRNAs, including miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, miRNA-138 and miRNA-19a, but expression levels of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 were significantly increased. [score:6]
Using qRT-PCR, we confirmed the down-regulation of miRNA-200b, miR-122, miR-19a, miRNA-466b, and miRNA-27a expression (Fig. 3 ). [score:6]
qRT-PCR measurements indicated that exposure of primary rat granulosa cells to Bt [2]cAMP for 24 h inhibited the expression of miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, and miRNA-138 and miRNA-19a while enhancing the expression of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 (Fig. 4 ). [score:5]
MiR-183, miR-96 and miR-19a were predicted to target the ABCA1 gene. [score:3]
We next evaluated the effects of Bt [2]cAMP stimulation of rat ovarian granulosa cells and of mouse MLTC-1 Leydig tumor cells on the expression of twelve miRNAs (miRNA-212, miRNA-122, miRNA-183, miRNA-200b, miRNA-466b, miRNA-182, miRNA-96, miRNA-27a, miRNA-132, miRNA-214, miRNA-138 and miRNA-19a) whose adrenal expression was differentially altered in response to treatment of rats with ACTH, 17α-E2 or DEX. [score:3]
More specifically, we assessed the impact of Bt [2]cAMP treatment on the expression of miRNA-212, miRNA-122, miRNA-27a, miRNA-466b, miRNA-200b, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96 and miRNA-19a. [score:3]
The levels of expression of miRNA-212, miRNA-122, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96, miRNA-466b, miRNA-200b, and miRNA-19a are shown. [score:3]
Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
Dexamethasone treatment decreased miRNA-200b, miR-122, miR-19a, miRNA-466b and miRNA27a levels, but increased miRNA-183 levels. [score:1]
0078040.g003 Figure 3Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
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[+] score: 29
Similarly, overexpression of each miR-17-92 cluster member decreased expression of corresponding voltage-gated potassium channel subunits (Fig. 5d), although Na [V]β1 expression was mostly unaffected by miR-19a. [score:7]
Significant mechanical allodynia was observed in rats overexpressing miR-18a, miR-19a, miR-19b or miR-92a, but not in those overexpressing miR-17 or miR-20a (Fig. 2e). [score:5]
L5 DRGs were obtained 28 days after SNL from rats injected with mixture of AAV vectors expressing antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a 7 days after SNL. [score:3]
AAV vectors expressing either a control AAV vector or mixture of AAV vectors encoding TuD antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a were administered 7 days after SNL. [score:3]
The number of putative target genes for miR-18a, miR-19a/b (miR-19a and miR-19b have the same seed sequence) and miR-92a were 695, 1,448 and 1,138, respectively (a total of 2,834 genes). [score:3]
Only the cluster members whose overexpression reduced the mechanical paw withdrawal threshold (miR-18a, miR-19a, miR-19b and miR-92a) were examined. [score:3]
In this context, therapeutic manipulation of miR-17-92 cluster would be advantageous, as its components miR-18a, miR-19a/b and miR-92a collectively modulate multiple potassium channel α subunits and auxiliary subunits in DRG neurons. [score:1]
As miR-19a/b and miR-92a have two predicted binding sites for Kcna4 3′-UTR and Kcnc4 3′-UTRs, respectively, both sites were mutated. [score:1]
Error bars are s. e. m. * P<0.05, ** P<0.01 and *** P<0.001 (K [V]1.1, P=0.014 for miR-17-92 and P=0.034 for miR-18a; K [V]1.4, P<0.001 for miR-17-92; K [V]3.4, P<0.001 for miR-17-92, P=0.047 for miR-19b and P=0.009 for miR-92a; K [V]4.3, P=0.031 for miR-17-92; K [V]7.5, P=0.002 for miR-17-92, P=0.048 for miR-19a and P=0.013 for miR-19b; DPP10, P=0.003 for miR-17-92 and P=0.043 for miR-92a; Na [V]β1, P=0.002 for miR-17-92 and P=0.030 for miR-19b), Dunnett’s test. [score:1]
Furthermore, the established mechanical allodynia was reversed by injection of a mixture of AAV vectors encoding antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a 7 days after SNL (Fig. 3b). [score:1]
Clone IDs of TuD were as follows: NC000001 (negative control), RH000611 (miR-17), RH000323 (miR-18a), RH000643 (miR-19a), RH000352 (miR-19b), RH000277 (miR-20a) and RH000184 (miR-92a). [score:1]
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[+] score: 26
Interestingly, siCx43 treatment induced a down-regulation of miR19a and miR224, which in turn, were not able to decrease AQP4 expression; *p < 0.05; values are represented as mean ± SEM. [score:6]
Therefore, the level of expression of AQP4 and Cx43 possibly affects the miR224 and miR19a with an opposite effect: a decrease of AQP4 is associated with an increase of both miRNAs and decrease of Cx43 is linked with a decrease of these miRNAs (Fig. 8). [score:3]
Figure 8Modulation of miR19a, miR23a, miR130a, miR224, miR381 and miR384-5p expression after siAQP4 and siCx43 treatment. [score:3]
In summary, we demonstrate for the first time that AQP4 decrease after siAQP4 induces an increase of miR224 and miR19a expression with decreases in Cx43 levels and astrocyte connectivity. [score:3]
Interestingly, even though not significant, miR19a, miR23a and miR384-5p exhibited an increased expression in the siAQP4 -treated animals of 47%, 36% and 15%, respectively. [score:3]
We found significant decreased expression of miR19a (44%) and miR224 (61%) in the ipsilateral cortex of siCx43 animals compared to siGLO control animals (Fig. 8B). [score:2]
However, siAQP4 and siCx43 injections appear to affect levels of miR224 and miR19a in opposite directions with an increase in the siAQP4 -treated cortex versus a decrease in the siCx43 brain. [score:2]
AQP4 Cx43 Homo sapiens Mus musculus Rattus norvegicus Homo sapiens Mus musculus Rattus norvegicus miR19a ● ● ● ● ○ ○ ○ miR23a ● ● ● ● ○ ○ ○ miR130a shown to repress transcriptional activity of AQP4 M1 promoter* ● ● ● miR224 ● ● ● ● miR381 ● ● ● ● miR384-5p ● ● ● ● ○ ○ ○● based on microrna. [score:1]
We chose to study 6 miRNAs, among those most conserved between species: miR19a, miR23a, miR130a, miR224, miR381, and miR384–5p. [score:1]
We chose the most conserved miRNAs between species and selected 6 miRNAs: miR19a, miR23a, miR130a, miR224, miR381, and miR384–5p (see Table 1). [score:1]
Therefore, interventions such as siAQP4 or miR224 and miR19a could be used as potential treatments to decrease levels of Cx43 in ALS and epilepsy. [score:1]
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[+] score: 24
In contrast, expression of miR-19a and miR-20a was downregulated in mouse NS cell differentiation. [score:6]
The possible role of miR-19a on cell survival, may explain why this miRNA was upregulated at early stages after the induction of mouse NS cell differentiation. [score:4]
The onset of miR-19a expression correlates with induction of proliferation during the first 3 days of differentiation (data not shown). [score:3]
Curiously, miR-19a expression was mostly increased during the first 3 days of differentiation, gradually decreasing toward control levels. [score:3]
Expression of specific proapoptotic (miR-16, let-7a and miR-34a) and antiapoptotic miRNAs (miR-20a and miR-19a) were analyzed by quantitative Real Time-PCR from 10 ng of total RNA using specific Taqman primers and GAPDH for normalization. [score:2]
Only limited information is available regarding the physiological role of miR-19a. [score:1]
However, additional studies are required to determine the specific role of both miR-20a and miR-19a during cell differentiation, and also evaluate if their expression is restricted to a specific cell type. [score:1]
In addition, the expression of antiapoptotic miR-19a and 20a was also evaluated. [score:1]
miR-19a and miR-20a are members of the miR-17-92 cluster [61], which consists of seven mature miRNAs, previously linked to tumorigenesis. [score:1]
Further, miR-19 appears to affect the level of proapoptotic protein Bim, thereby preventing apoptosis and promoting cell survival. [score:1]
Recently, additional functions have been assigned to this cluster, particularly to miR-20a and miR-19a. [score:1]
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[+] score: 20
Based on functional and pathway analysis and related literature examination, we selected miR-134-5p, miR-207, and miR-465-5p to represent the up-regulated miRNAs, and miR-30b-5p, miR-19a-3p, and miR-130a-3p to represent the down-regulated miRNAs. [score:7]
Among these DEmiRNAs, 6 up- or down-regulated miRNAs were chosen for further analysis, including miR-134-5p, miR-207, miR-465-5p, miR-30b-5p, miR-19a-3p, and miR-130a-3p. [score:4]
The DEmiRNAs (e. g., miR-134-5p, miR-207, miR-465-5p, miR-30b-5p, miR-19a-3p, and miR-130a-3p) and common target genes, such as Chst1 and Nrbf2, may be strongly associated with the pulmonary inflammation induced by ZnO-NPs. [score:3]
In our network, Chst1 (carbohydrate sulfotransferase 1) is regulated by four miRNAs, including miR-30b-5p, miR-19a-3p, miR-130a-3p, and miR-134-5p, while Nrbf2 (nuclear receptor binding factor 2) is regulated by miR-30b-5p, miR-19a-3p, miR-130a-3p, and miR-207. [score:3]
Additionally, in our study, Nrbf2 was regulated by miR-30b-5p, miR-19a-3p, miR-130a-3p, and miR-207. [score:2]
Chst1 is modulated by four miRNAs, including miR-30b-5p, miR-19a-3p, miR-130a-3p, and miR-134-5p. [score:1]
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[+] score: 17
In input samples, all three miRNAs examined (miR-34a, miR-19a, miR-326) showed enhanced expression 30 min post-HFS and decreased expression below the contralateral control level when HFS was given in the presence of AP5 (Figure 4A). [score:5]
Target gene list sizes for miRNAs with activity -dependent association with Ago2 for the 8 enhanced miRNAs were 97 (miR-20a), 156 (miR-219), 58 (miR-223), 114 (miR-29b), 30 (miR-330), 91 (miR-34a), 156 (miR-384), and 53 (miR-592) and for the 5 depleted miRNAs were 52 (let-7f), 55 (miR-338), 47 (miR-212), 255 (miR-19a), 32 (miR-326). [score:3]
When comparing miRNA Ago2/input expression ratios, eight miRNAs (miR-384, miR-29b, miR-219, miR-592, miR-20a, miR-330 miR-223, and miR-34a) exhibited increases relative to the contralateral dentate gyrus, whereas five miRNAs (miR-let7f, miR-338, miR-212, miR-19a, and miR-326) showed decreases in this ratio. [score:3]
When AP5 was infused prior to HFS, the Ago2/IP expression ratio of miR-19a and miR-326 was increased, indicating NMDAR -dependent dissociation of these miRNA from Ago2 (Figure 4C). [score:3]
In contrast, miR-19a showed no change and miR-326 had a significantly decreased Ago2/IP expression ratio following HFS. [score:3]
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[+] score: 16
Van Almen et al. [29] reported that decreased hsa-miR-19 expression leads to increased expression of CTGF and TSP-1 in aged failure-prone hearts. [score:5]
The miRNAs hsa-miR-19a (12 degrees) and hsa-miR-19b (12 degrees) were significantly down-regulated in the DCM samples. [score:4]
Previous studies show that miRNA-19a and 19b are members of the miR-17-92 cluster, which regulates the expression of ECM proteins CTGF and TSP-1 in the ageing-related heart failure process [35]. [score:4]
In the network, the performance differences in the most critical miRNAs (hsa-miR-340, hsa-miR-19a, hsa-miR-19b, etc. ) [score:1]
The miRNAs hsa-miR-200b (16 degrees), hsa-miR-181c (14 degrees), hsa-miR-340 (13 degrees), hsa-miR-557 (13 degrees), hsa-miR-19a (12 degrees), hsa-miR-19b (12 degrees) and hsa-miR-548f (12 degrees) were significantly differentially regulated in DCM samples compared with non-failing control samples. [score:1]
The key miRNAs identified included hsa-miR-181c, hsa-miR-19a and hsa-miR-19b, which all have higher degrees in the network diagram. [score:1]
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[+] score: 16
Accessing the detailed page, we further acquired that miR-19a regulates H3K4me3 states of the miR-17-92 cluster through directly targeting Egr2 and Jardi1b and influences DNA methylation of H3R8 and H4R3 by repressing PRMT5. [score:5]
Similarly, the epigenetic modifications that can affect miR-19a could be searched in the ‘Epigenetic Modification Affects miRNA Expression’ section. [score:3]
The searching result page shows nine records indicating that H3K4me3, H3K79me2, histone acetylation and DNA methylation can all affect miR-19a expression in diverse conditions (Figure 2b). [score:3]
To this end, we merged the aforementioned regulatory information and created a molecular network to reflect the interaction between miR-19a and diverse epigenetics (Figure 2c). [score:2]
Taking miR-19a as an example, we learned that miR-19a can both affect H3K4me3 states in human macrophage and control DNA methylation modification of human leukemia and lymphoma cells through querying in the ‘MiRNA Regulates Epigenetic Modifications’ section (Figure 2a). [score:2]
Figure 2. Searching result and integrated network of ‘miR-19a’. [score:1]
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[+] score: 13
Since co-expressed miRNAs have been shown to coordinately regulate canonical cell signaling networks associated with cell death and cell survival [18], it is notable that we found that all members of the miR-17-92 cluster (miR-17-5p, miR-18a, miR-19a, miR-92a) are upregulated after TBI and these miRNAs co-target and possibly negatively co-regulate many TBI-altered genes. [score:10]
Microfluidic analysis of laser captured neurons has never been reported; in this proof-of-principle experiment, although differences did not reach statistical significance due to the stochastic variability in the six 30 cell pools of dying or surviving neurons, we detected a trend in increased expression of miR-15b and miR-19a in dying neurons. [score:3]
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[+] score: 10
Notably, we found miR-222, miR-291-3p, miR-183, miR-363-3p, miR-92, miR-19a and miR-145 as down-regulated miRNAs between E11 and E13 and whose expression was negatively correlated with the expression of their predicted targets. [score:10]
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[+] score: 10
Furthermore, fecal colonocytes from the tumor bearing AOM rats showed a significantly higher induction of miR-34a, miR-18a, miR-19a and miR-142-3p (3.0, 2.3, 2.2 and 2.1 fold induction respectively) (p<0.05), Thus, it is evident that the miRNA dysregulation in the histologically normal colonic mucosa of the AOM rats was mirrored in the fecal colonocytes and the miRNA modulation was augmented by the presence of neoplasia in the colon thus supporting potential role as a minimally intrusive modality for field carcinogenesis detection. [score:2]
We noted that miRNAs miR-34a, miR-18a, miR-19a, miR-32, miR-96, miR-142-3p miR-29b and miR-7b were significantly upregulated in the AOM rat fecal colonocytes compared to those obtained from the saline controls and the degree of induction was greater in the tumor bearing AOM rats compared to the tumor non-bearing AOM rats (Fig. 3B). [score:2]
In the 16 week colonic biopsies, we observed that while all miRNAs trended to increase (versus age-matched saline treated animals) although only 7 miRNAs (miR-34a, miR-21, miR-18, miR-376a, miR-19a, miR-9 and miR-29b) achieved statistical significance (fold inductions of 1.73, 2.72, 2.15, 2.26, 2.18, 1.53, and 1.71,respectively) (Table 2). [score:1]
We further attempted LASSO (least absolute shrinkage selection operator) approach among the ten markers and found three microRNAs (miR-21, miR-18a, and miR-19a) as the most sensitive. [score:1]
Similarly, in the fecal colonocytes, the miRNAs miR-34a, miR-18a and miR-19a, showed an AUROC of 0.926, 0.918 and 0.968, respectively. [score:1]
Based on these criterion miR-21 achieved distinguished predictive ability with a 0.914 AUC, miR-18a and miR-19a achieved excellent predictive ability with a 0.877 and 0.872 AUC respectively, miR-29b achieved an almost excellent predictive ability with a 0.789 AUC. [score:1]
Out of the 12 miRNAs tested, four (miR-21, miR-18a, miR-29b, and miR-19a) were significantly different between AOM and Saline group (p<0.02). [score:1]
Out of the 12 miRNAs tested, miR-21 and miR-19a showed statistically significant differences (2.19 and 2.79 fold induction respectively) in the tumor bearing and non-bearing AOM rats. [score:1]
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[+] score: 7
Other miRNAs from this paper: hsa-mir-19a
A significant decrease in CUL5 expression is observed in the majority of breast cancers [19, 20], while inhibition of CUL5 expression using microRNA-19a and -19b induced cervical carcinoma cell proliferation and invasion [21]. [score:7]
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[+] score: 7
Jiang W. L. Zhang Y. F. Xia Q. Q. Zhu J. Yu X. Fan T. Wang F. MicroRNA-19a regulates lipopolysaccharide -induced endothelial cell apoptosis through modulation of apoptosis signal -regulating kinase 1 expression BMC Mol. [score:4]
Another miRNA that targets ASK1, miRNA-19a, also showed an anti-apoptotic effect under lipopolysaccharide stimulation in endothelial cells [34]. [score:3]
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[+] score: 7
Busch et al. found that the inhibition of miR-19a-3p with an antagomir led to an increase in 5-LO mRNA expression in T lymphocytes 46. [score:5]
MiR-19a-3p has been reported to inhibit breast cancer progression and metastasis by inducing macrophage polarization 45. [score:2]
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[+] score: 6
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-19b-2, rno-mir-27a, rno-mir-217
org/)] were used, and four miRs (i. e., miR-19a, miR-19b, miR-27a, and miR-217) were predicted to target the 3′-untranslated region (3′ UTR) of GRK6 according to the score (the sequence comparison is shown in Supplementary Fig. S3a). [score:5]
The sequences of the rno-miR-27a mimics were: 5′-UUC ACA GUG GCU AAG UUC CGC-3′ and 5′-GGA ACU UAG CCA CUG UGA AUU-3′; rno-miR-19a mimics were: 5′-UGU GCA AAU CUA UGC AAA ACU GA-3′ and 5′-AGU UUU GCA UAG AUU UGC ACA UU-3′; rno-miR-19b mimics were: 5′-UGU GCA AAU CCA UGC AAA ACU GA-3′ and 5′-AGU UUU GCA UGG AUU UGC ACA UU-3′; rno-miR-217 mimics were: 5′-UAC UGC AUC AGG AAC UGA CUG-3′ and 5′-AGU CAG UUC CUG AUG CAG UAU U-3′. [score:1]
[1 to 20 of 2 sentences]
[+] score: 6
miR-17 is a member of the miR-17/92 cluster, one of so far, the best-studied microRNA clusters that codes six mature miRNAs: miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1. Members of this cluster are expressed in a variety of tissues and carry out essential functions both in normal development and in diseases. [score:6]
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[+] score: 6
While the reduction in expression of miR-17-5p, miR-18a, miR-20a, and miR-92 were well coordinated in transdifferentiation, the expression of miR-19a was not concordant with its neighboring microRNA genes. [score:5]
The genes encoding for miR-17-1/miR-17-5p, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1 are clustered on chromosome 15 [35]. [score:1]
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[+] score: 6
The mir-17 family is the one most enriched (p = 3.24 E-4; Table S6) and comprises mir-17, mir-18a, mir-19a, mir-20a, mir-19b-1 and mir-92-1. This family is expressed as polycistronic units, revealing a common regulatory mechanism [62], that is confirmed by the similarity of their expression profiles (Figure 4 D). [score:6]
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[+] score: 5
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
First, a subgroup of miRNAs (miR-15b-5p, miR-17-5p, miR-18a-5p, miR-19a-3p, miR19b-3p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23b-5p, miR-24-3p, miR-27a-3p, miR-92a-3p, miR-93-5p, miR-142-3p, miR-344b-2-3p, miR-431, miR-466b-5p and miR-674-3p) displayed increased expression levels during latency (4 and 8 days after SE), decreased their expression levels at the time of the first spontaneous seizure and returned to control levels in the chronic phase (Fig. 2, Supplementary Fig. S1). [score:5]
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[67] On the other hand, MECP2, a transcriptional regulator targeted by miR-19, miR-30e and miR-365, binds to methylated DNA and has been shown to contribute to early life stress -dependent epigenetic programming of HPA axis -associated genes. [score:4]
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MicroRNAs like miR-19a, 34b, 129, 135a, 142-3p, miR-153, miR-186, miR-187, and miR-301a were significantly downregulated in Cs1-ko mice. [score:4]
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Some up-regulated miRNAs such as miR-19a, miR-24 and miR-128a were unchanged at the level of their primary transcripts. [score:4]
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In addition, the miR-17-19 cluster, which comprises seven miRNAs (miR-17-5p, miR-17-3p, miR-18, miR-19a, miR-20, miR-19b, and miR-92-1) and promotes cell proliferation in various cancers, has been demonstrated to be significantly upregulated at the clonal expansion stage of adipocyte differentiation. [score:4]
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This miR-19a/b family acts as a key regulator of cardiac hypertrophy and apoptosis. [score:2]
We found that miR-99, miR-100, miR-208, miR-181, miR-19 and many others were associated to cardiac hypertrophy and apoptosis. [score:1]
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In our previous study [12], we found that miR-17, miR-19a, miR-20a, miR-19b and miR-92a, but not miR-18a, were highly expressed in the heart of C57BL/6 mice. [score:3]
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The following miRNAs, also present in the VTMs list of Fig 5, were found by RT-PCR to be dysregulated in mouse lung tissue: miR-21, miR-146, miR-20, miR-302, miR-19, miR-98, let-7a, miR-15a. [score:2]
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Among the spleen-specific miRNAs identified, five of them belong to the mir17 miRNA cluster, which comprise miR-17, miR-18, miR-19a, miR-19b, miR-20, miR-25, miR-92, miR-93, miR-106a, and miR-106b [59]. [score:1]
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Both miR-17 and miR-19, as representatives of the miR-17-92 cluster, were tested in all tissues, but no changes were observed between controls and aGvHD rats (data not shown). [score:1]
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MicroRNA profiling identified several miRNAs that have been previously associated with cardiac hypertrophy such as miR-214, miR-23b, miR-15b, rno-miR-26b, rno-miR-221, rno-miR-222, rno-miR-107 [59], miR-23a, miR-208, rno-miR-133b, miR-19a and mi-r133a [60]. [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
The miR-17-92 cluster (polycistronic miRNA gene) encodes six miRNAs (miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92-1) located in the third intron of a ~7-kb primary transcript known as C13orf25 [61]. [score:1]
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For instance, it was reported that the treatment of human embryonic stem (ES) cells with activing A plus basic fibroblast growth factor (bFGF) induced the repression of Nurr1 along with the induction of several miRNAS, of which miR-302d, miR-217, miR-19a and miR-372, specifically repressed a luciferase reporter gene fused to the 3’UTR of human Nurr1 [24]. [score:1]
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MiR-17-5p belongs to the miR-17~92 cluster, located on the human chromosome 13q31, and is a prototypical example of a polycistronic miRNA gene encoding six miRNAs (miR-17-5p, miR-18, miR-19a, miR-19b, miR-20 and miR-92). [score:1]
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The miR-17-92 cluster is among the best-explored miRNA clusters, including six members (miR-19a, -19b, -17, -18a, -20a, -92a). [score:1]
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hsa-mir-17 belonged to a polycistronic cluster (also containing hsa-mir-18a, hsa-mir-19a, and hsa-mir-20a) residing in a large genomic region highly enriched with TF binding sites, let-7a and let-7f, also likely to be transcriptionally coupled, were also enriched with TFBSs, and mir-7-1 was also found in a large genomic region with high density of TFBSs. [score:1]
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